Vol 9: Role of Nitric Oxide Synthases in Early Blood-Brain Barrier Disruption following Transient Focal Cerebral Ischemia. - Download this document for free, or read online. Document in PDF available to download.

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Vol 9: Role of Nitric Oxide Synthases in Early Blood-Brain Barrier Disruption following Transient Focal Cerebral Ischemia.This article is from PLoS ONE, volume 9.AbstractThe role of nitric oxide synthases NOSs in early blood-brain barrier BBB disruption was determined using a new mouse model of transient focal cerebral ischemia. Ischemia was induced by ligating the middle cerebral artery MCA at its M2 segment and reperfusion was induced by releasing the ligation. The diameter alteration of the MCA, arterial anastomoses and collateral arteries were imaged and measured in real time. BBB disruption was assessed by Evans Blue EB and sodium fluorescein Na-F extravasation at 3 hours of reperfusion. The reperfusion produced an extensive vasodilation and a sustained hyperemia. Although expression of NOSs was not altered at 3 hours of reperfusion, L-NAME a non-specific NOS inhibitor abolished reperfusion-induced vasodilation-hyperemia and significantly reduced EB and Na-F extravasation. L-NIO an endothelial NOS eNOS inhibitor significantly attenuated cerebral vasodilation but not BBB disruption, whereas L-NPA and 7-NI neuronal NOS nNOS inhibitors significantly reduced BBB disruption but not cerebral vasodilation. In contrast, aminoguanidine AG an inducible NOS iNOS inhibitor had less effect on either cerebral vasodilation or BBB disruption. On the other hand, papaverine PV not only increased the vasodilation-hyperemia but also significantly reduced BBB disruption. Combined treatment with L-NAME and PV preserved the vasodilation-hyperemia and significantly reduced BBB disruption. Our findings suggest that nNOS may play a major role in early BBB disruption following transient focal cerebral ischemia via a hyperemia-independent mechanism.

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